Chronic inflammation in benign prostate tissue is associated with high-grade prostate cancer in the placebo arm of the prostate cancer prevention trial.
Chronic inflammation in benign prostate tissue is associated with high-grade prostate cancer in the placebo arm of the prostate cancer prevention trial.
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良性前列腺组织中的慢性炎症与前列腺癌预防试验的安慰剂组中的高级前列腺癌有关。
DOI：
10.1158/1055-9965.epi-13-1126
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发表时间：
2014-05
期刊：
影响因子：
--
通讯作者：
Platz EA
中科院分区：
文献类型：
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作者：
Gurel B;Lucia MS;Thompson IM Jr;Goodman PJ;Tangen CM;Kristal AR;Parnes HL;Hoque A;Lippman SM;Sutcliffe S;Peskoe SB;Drake CG;Nelson WG;De Marzo AM;Platz EA
慢性炎症被认为会影响前列腺癌的发展，尽管还没有确定的联系。前列腺癌病例(N=191)在原因(临床指示)或研究结束(方案指导)活组织检查中被发现，而频率匹配的对照(N=209)在研究结束活组织检查中被定义为癌症阴性，样本来自前列腺癌预防试验的安慰剂组。用H&E染色切片的数字图像直观地评估活检核心良性区域的炎症患病率和程度。用Logistic回归估计关联度。86.2%的病例和78.2%的对照组至少有一个活检核心(3个评估)，其中良性区域有炎症，其中大部分是慢性炎症。至少有一个有炎症的活检核心的男性患前列腺癌的几率是那些没有炎症核心的男性的1.78倍(95%可信区间为1.04-3.06)。高级别疾病的关联性更强(Gleason sum 7-10，N=94；优势比[OR]=2.24，95%可信区间1.06-4.71)。这些模式仅限于前列腺炎性疾病患者和对照组，在这些患者和对照组中，前列腺炎性疾病对活检建议的影响最小，因为他们的PSA较低(活检时为2 ng/ml)。炎症，其中大部分是慢性的，在良性前列腺组织中很常见，与前列腺癌，特别是高级别前列腺癌呈正相关。这种关联似乎不是由于检测偏差造成的。这项研究支持炎症和前列腺癌发生之间的病因学联系，并提出了一种通过减轻前列腺癌内炎症来预防的途径。
Chronic inflammation is hypothesized to influence prostate cancer development, although a definitive link has not been established. Prostate cancer cases (N=191) detected on a for-cause (clinically indicated) or end-of-study (protocol directed) biopsy, and frequency-matched controls (N=209), defined as negative for cancer on an end-of-study biopsy, were sampled from the placebo arm of the Prostate Cancer Prevention Trial. Inflammation prevalence and extent in benign areas of biopsy cores were visually assessed using digital images of H&E stained sections. Logistic regression was used to estimate associations. 86.2% of cases and 78.2% of controls had at least one biopsy core (of 3 assessed) with inflammation in benign areas, most of which was chronic. Men who had at least one biopsy core with inflammation had 1.78 (95% CI 1.04–3.06) times the odds of prostate cancer compared with men who had zero cores with inflammation. The association was stronger for high-grade disease (Gleason sum 7–10, N=94; odds ratio [OR]=2.24, 95% CI 1.06–4.71). These patterns were present when restricting to cases and controls in whom intraprostatic inflammation was the least likely to have influenced biopsy recommendation because their PSA was low (<2 ng/mL at biopsy). Inflammation, most of which was chronic, was common in benign prostate tissue, and was positively associated with prostate cancer, especially high-grade. The association did not appear to be due to detection bias. This study supports an etiologic link between inflammation and prostate carcinogenesis, and suggests an avenue for prevention by mitigating intraprostatic inflammation.